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Pathology-Cardio > Valvular diseases > Flashcards

Valvular diseases Flashcards

1
Q

when does a valve close?

A

when back-flow pressure is greater than chamber pressure

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2
Q

when does a valve open?

A

chamber pressure is greater than out-flow pressure

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3
Q

what does directional flow depend on?

A

competency of valves

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4
Q

which valves are subject to greater greater mechanical abrasions?

A

pulmonic and aortic

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5
Q

why is velocity through semilunar valves greater?

A

due to smaller openings and greater chamber pressures

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6
Q

mitral stenosis

A

•Rheumatic heart disease
•Remarkably well tolerated
•Atrial enlargement associated
with atrial fibrillation

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7
Q

aortic stenosis

A
  • Aging (senile calcification)
  • Biscuspid aortic valve
  • Rheumatic heart disease
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8
Q

mitral regurgitation

A

•Mitral valve prolapse
•Advanced stenosis (fish
mouth) - RHD
•Ruptured papillary muscle

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9
Q

aortic regurgitation

A
  • Advanced valvular distortions

* Syphilitic aortitis

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10
Q

what murmurs are heard in systole?

A

AS

MR

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11
Q

what murmurs are heard during diastole?

A

AR

MS

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12
Q

machinery murmur is

A

patent ductus arteriosus

-switches directions

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13
Q

what side of lesion is more significant?

A

left

-means increased pressures

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14
Q

why are aortic valves more significant than mitral?

A

-sudden decompensation of aortic valve leads to death
-syncope due to aortic stenosis presages sudden death
-stenosis leads to left ventricular hypertrophy
-significance due both to effects on systemic outflow and
coronary flow

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15
Q

“jet streams” are associated with

A

AS

  • can damage vessels
  • allow thrombosis and bacterial deposition
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16
Q

what cause left sided lesions?

A
  1. Mitral valve prolapse
  2. Aortic stenosis
    - congenital bicuspid valve
    - rheumatic fever (also mitral stenosis)
    - senile calcifications
  3. Congenital malformations – VSD
  4. Infectious endocarditis
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17
Q

what cause right sided lesions?

A
  1. congenital lesions
  2. intravenous drug use (infectious)
  3. systemic diseases (Lupus) – both right and left
    valvular lesions
  4. carcinoid syndrome
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18
Q

Aortic stenosis

A

-Tricuspid aortic valve>bicuspid>rheumatic fever
(10%)
-65/75/85 – 2/3/4
-Normal aging – calcification
-presents in 8-9th decade
-Rheumatic heart disease – most commonly presents
as aortic stenosis (tricuspid) in adults <70
-decreasing in recent years
-Valve replacement when cardiac output is
insufficient

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19
Q

AS: bicuspid aortic valve

A

-1-2% of population; 2X more common in males
-familial; autosomal dominant with variable
penetrance
-early calcification and stenosis of aortic valve
-“heaped up” calcifications interfere with function
-presents 6th – 7th decade
-calcification of tricuspid valve presents later
-progressive stenosis; late regurgitation

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20
Q

cardiac symptoms of Mitral valve prolapse

A

-mitral regurgitation (significant if greater than
15%)
-supraventricular arrhythmias/palpitations –
particularly with atrial enlargement secondary to
regurgitation
-sudden death
-bacterial endocarditis (no longer indication for
dental prophylaxis)

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21
Q

clinical findings with mitral valve prolapse?

A
  • mid to late systolic clicks
  • continuous or crescendo systolic murmur
  • syncope requires further investigation
22
Q

MVP syndrome/dysautonomia

A
  • chest pain, dyspnea, fatigue, dizziness, near syncope, anxiety,
  • life style modifications, education and re-assurance
23
Q

myxomatous degeneration with MVP

A

-excessive mucopolysaccharides, stretching of
valve leaflets
-genetic variants of fibrillin, elastin, and collagen
(Marfan’s, Ehler’s-Danlos)
-anorexia, dehydration in some women that is
reversible
-increased mitral valve surface area with
prolapse into left atrium during systole

24
Q

rheumatic heart disease

A
  • S. pyogenes
  • untreated strep pharyngitis in children
  • is main cause of death from heart disease in ages 5-25
  • associated with pharyngitis, PSGN, impetigo (GAS)
25
Q

autoimmune reaction in rheumatic heart disease

A

-several weeks after severe pharyngitis
-antibodies to hyaluronate in Strep capsules cross
react with glycoproteins in heart valves
-antibodies to streptolysin O good indicator of
severity of disease
-cross-reaction to streptolysin M; different M types
may have different potential for RF
-associated with specific HLA types

26
Q

pathogenesis of rheumatic heart disease

A

-lesions sterile and do not result from direct
bacterial invasion
-rate of development increases with severity of the
initial Strep infection
-individual susceptibility may be related to
genetically determined immune response genes to
Strep antigens

27
Q

acute rheumatic fever

A
  1. Pancarditis
    -Myocarditis
    -Pericarditis
    -Valvular disease
    -Mitral valve > aortic valve
    -Valvular insufficiency; mitral insufficiency most
    commonly involved in acute heart failure
28
Q

rheumatic fever: aschoff bodies

A
  • pathognomonic of rheumatic fever
  • collections of reactive histiocytes
  • around blood vessels
29
Q

rheumatic fever: anitschkow myocytes

A
  • actually HISTIOCYTES
  • not limited to rheumatic fever: occur with any form of inflammation of heart
  • cardiac histiocytes
  • caterpillar chromatin pattern
30
Q

what percent develops chronic valvular disease in rheumatic heart disease?

A

65-75%
Chronic inflammatory reaction leading to fibrosis and
thickening of valvular - stenosis
-mitral > aortic&raquo_space;>tricuspid
-leads to fusion (2-10 years), stenosis +/- insufficiency
-becomes clinically apparent after several decades
-most common cause of mitral (99%); 10% of aortic stenosis

31
Q

what clinical consequences result from chronic valvular disease?

A

include atrial enlargement with
atrial fibrillation, LVH, systolic and diastolic murmur,
hemolytic anemia, and pulmonary hypertension

32
Q

bacterial endocarditis presentation

A

fever
heart murmur
fatigue

33
Q

most common presentation of bacterial endocarditis

A

FEVER OF UNKNOWN ORIGIN

34
Q

bacterial endocarditis: left sided emboli

A
  1. Osler’s nodes
  2. Janeway lesions
  3. Brain abscesses
  4. multiple right sided pulmonary emboli)
    - multiple blood cultures (negative in fungal)
    - long-term antibiotic therapy
35
Q

organisms that can cause bacterial endocarditis

A 
95% bacteria 
1.Strep
2.Viridans
3.Staph
-enterococci
-pneumococci
-G- rods
5% rickettsia, chlamydia, fungal
36
Q

predisposing conditions

A
  • any anomaly leading to abnormal flow, shunting (particularly right to left through septal defects), exposure of collagen, or damage to valves (fibrin deposition)
  • IV drug use predisposes to right-sided infections (S. aureus, Candida, Aspergillus)
37
Q

where does most endocarditis occur on?

A

left sided

38
Q

acute endocarditis

A

-S. aureus
-normal valves
-can occur on right, especially with IV drug use
(right>left)
-high fever, new onset murmur
-rapidly progressive lesions, very destructive
-fenestrations, distortions
-destructive lesions of aortic valve lead to sudden
death

39
Q

sub-acute endocarditis

A

S. viridans
-abnormal valves
-left>right (almost never on right)
-low or no fever, new onset murmur, slowly
progressive lesions
-antibiotic prophylaxis for dental procedures
and surgery only for prosthetic valves, previous
endocarditis or specific congenital defects

40
Q

IV drug use endocarditis

A

-Right > left or bilateral

41
Q

organisms that cause endocarditis in IV drug users

A
  • S. aureus most common
  • gram negatives or multiple (including Pseudomonas)
  • fungi
  • Candida, aspergillus
42
Q

what are the vegetations seen in endocarditis?

A

-Mixture of bacteria, fibrin, thrombosis,
inflammatory cells
-Deposition on valve surface; enhanced by prior
damage or NBTE
-Local proliferation of bacteria
-Structural damage with Staph aureus
-Emboli to brain, peripheral circulation (Osler’s
nodes, Janeway lesions)
-Flow side; edge of cusps

43
Q

non-bacterial thrombotic endocarditis

A
  • Sterile lesions; no bacteria

- Deposition of platelets, thrombin

44
Q

what is associated with NBTE

A
  • SLE – Libman Sacks endocarditis
  • Cancer – pancreatic carcinoma (migrating
    thrombophlebitis) (pro-coagulant state)
45
Q

SLE – Libman Sacks endocarditis

A

-vegetations on the mitral and tricuspid valves (NBTE)
-occur in approximately half the cases of SLE
-unlike rheumatic heart disease, often involves valves on
the RIGHT side of the heart
-composed of necrotic debris, fibrinoid material,
disintegrating fibroblasts and inflammatory cells
-small (usually 1-4 mm); usually occur on flow side of
leaflets, but can occur behind them
-dysfunction results in regurgitation
-? associated with anti-phospholipid syndrome

46
Q

which valves does Libman Sacks endocarditis usually involve?

A

right side of heart

47
Q

Carcinoid tumors

A

-Neuroendocrine-derived tumor of the GI tract,
lungs that secrete vaso-active substances
(serotonin, kallikrein)
-Flushing, diarrhea

48
Q

where are Carcinoid tumors most common?

A

Most common site of involved primary tumor is
in the small intestine (ileum) where it
metastasizes to the liver (appendix more
common, but doesn’t metastasize)

49
Q

Carcinoid syndrome

A

-Valvular associated only with metastasis to
liver and secretion of substances into the
hepatic vein (to right heart and lungs)
-affect only the right side of the heart –
metabolized in the lung and never make it to the
left side
-Primarily thickening of the valve with various
degrees of stenosis

50
Q

in Carcinoid syndrome, which valve is most commonly affected?

A

tricuspid valve

51
Q

artificial valves

A 
-Valve replacement required for stenosis 
(M/A) or severe regurgitation (A)
-Artificial or natural
-Associated with thrombosis
-Long-term anticoagulation
-Associated with infection, including Staph 
epidermidis
-Often need to be replaced

Pathology-Cardio (11 decks)

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